Korean J Physiol Pharmacol.
1998 Dec;2(6):763-770.
Effect of endothelin-1 on proliferation and differentiation of rat
tracheal epithelial cells
- Affiliations
-
- 1Department of Physiology, College of Medicine, Pusan National University, 1-10 Ami-Dong, Suh-Gu, Pusan 602-739, Korea.
Abstract
-
A number of substances involved in the proliferation and
differentiation of the tracheobronchial epithelium have been
identified. The defects in the control of the proliferation and
differentiation of tracheobronchial epithelial cells appear to
constitute crucial steps in the transition of normal cells to
neoplastic ones. Endothelin-1 is produced by tracheal epithelial cells,
and its receptors are present in tracheal epithelial cells. However,
the effect of endothelin-1 on the proliferation and differentiation of
tracheal epithelial cells has not been clearly elucidated. This study
was undertaken to investigate these actions of endothelin-1 in primary
cultured cells of rat tracheal epithelia. Endothelin-1 stimulated
proliferation of tracheal epithelial cells 1.5-fold when compared with
that of control cells. Endothelin-1 increased mitogen-activated protein
kinase (MAPK) activity. Herbimycin A, a tyrosine kinase inhibitor,
inhibited endothelin-1-induced proliferation of epithelial cells. The
treatment of endothelin-1 during the primary culture of tracheal
epithelial cells increased AB-PAS-stained cell population and ciliated
cell population 6.5 fold and 1.5 fold, respectively, when compared with
those in control cells. The responsiveness to carbachol and forskolin
in the Cl- secretion was increased 1.7 and 1.9 fold, respectively, in
the endothelin-treated epithelial cells. These results indicated that
endothelin-1 increases proliferation via MAPK pathway and stimulates
differentiation to secretory and ciliated cells in rat tracheal
epithelial cells.